子宫蠕动波在胚胎着床中起重要作用，但其调控机制不清。一般认为，子宫中存在类似胃肠道Cajal间质细胞的起搏细胞——Telocytes，通过缝隙连接激发子宫平滑肌细胞产生收缩运动，但目前尚不明确Telocyte调控子宫收缩的机制。本课题创新性地提出子宫Telocytes作为雌激素感受器，通过非基因组途径激活T型钙通道，产生膜电位变化，进而调控子宫平滑肌收缩的假说。拟通过比较子宫Telocytes在雌激素、雌激素核受体拮抗剂、T型钙通道特异性阻断剂的作用下，Telocyte中T型Ca2+通道电流、细胞内Ca2+浓度及膜电位变化，揭示人类子宫肌层中Telocytes将雌激素信号转化为平滑肌收缩效应的机制。本研究将子宫Telocytes与子宫蠕动波相联系，对抑制异常子宫蠕动波提供干预靶点和理论依据，以期改善胚胎移植后妊娠结局。

Uterine peristalsis plays an important role in embryo implantation. However, its origin and regulation mechanism remains unclear. Telocytes, the ‘interstitial Cajal-like cells’ out of digestive canal, are located in uterus and its membrane depolarization could spread into neighbouring smooth muscle cells through gap junctions to activate contraction. However, the mechanism of Telocytes regulating uterine contraction is still blank. Here, we put forward a hypothesis that Telocytes are sensors of estrogen level, and they could activate T-type Ca2+ channel through non-genomic signalling events, increase intracellular Ca2+ level, raise membrane potential, finally induce myometrium contraction. Thus, studies are designed to observe influence of estrogen on the current of T-type Ca2+ channel, intracellular Ca2+ concentration and membrane potential changes in uterine telocytes. In conclusion, this study aims at revealing the mechanism of uterine telocytes transforming estrogen signal into uterine contraction, providing a target in inhibiting abnormal uterine peristalsis and improveing embryo transfer outcome.